Although the in vivo properties of basic fibroblast growth factor is unknown, and nothing is known about its regulation at the transcriptional or translational levels or about its release, the in vitro mitogenecity of FGF for fibroblasts, smooth muscle cells and especially for endothelial cells, raises the possibility that it is important in wound healing and angiogenesis. To produce myocardial necrosis without contamination by blood borne elements such as platelets or white cells which might contain growth factors, rats hearts were exposed to 60 minutes of ex vivo incubation in saline at 24 degrees. To assay this tissue it was necessary to develop a sensitive and specific RIA for basic FGF using polyclonal antisera raised against synthetic peptides representing aminoacids 1 to 24 and 33 to 43 of basic FGF. A wide variety of extraction conditions and RIA buffers were used to maximize sensitivity. Specificity was partially confirmed by parallel curves using serial dilutions of homogenized heart and additions of recombinant basic FGF to RIA buffer and to homogenized heart. Further proof of the specificity in this assay is being sought using western blotting and non denaturing techniques such as gel filtration and immunoprecipitation. With this radioimmunoassay the normal rat heart was found to contain approximately 9 mg per gram while the infarcted hearts contained twice that amount. The mitogenecity of the necrotic myocardium was only mildly enhanced compared to that of controls, suggesting that the FGF immunoreactivity may not be completely indicative of enhanced bioavailability. Alternatively myocardial necrosis may result in the release of growth inhibitors such as acidosis, hyperkalemia or specific polypeptides.